The increase in stroke volume observed in physcial training is the result of an increase in end-diastolic ventricular volume. In the exercise-trained animal, the increased diastolic volume is associated with an increase in muscle mass. The changes in ventricular volume can be primarily caused by an increase in the level of parasympathetic nervous system activity and a decrease in the sympathetic nervous system activity. The inotropic response of the ventricle is not affected by training even though there is a selective neurogenic control on the chronotropic response. The atrial contribution to ventricular filling is augmented and will further affectively increase stroke volume. An early change in the coronary vascular bed suggests an increase in the size or number of coronary vessels and a possible redistribution of coronary flow across the heart. Through the increase in coronary bed size, the overall coronary reserve capacity can be increased. This would constitute a beneficial effect of training to the organism. The decrease in the role of the sympathetic nervous system response to apparent reflex activation will decrease the release of catecholamines in the heart. Using the chronically instrumented conscious animal, the changes in size and distribution of coronary flow will be ascertained. Changes in autonomic nervous system balance will be sought. The experiments are directed toward an understanding of the underlying basic mechanisms in the cardiac response to exercise training.